Haves and have nots must find a better way: the case for open scientific hardware

Many efforts are making science more open and accessible; they are mostly concentrated on issues that appear before and after experiments are performed: open access journals, open databases, and many other tools to increase reproducibility of science and access to information. However, these initiatives do not promote access to scientific equipment necessary for experiments. Mostly due to monetary constraints, equipment availability has always been uneven around the globe, affecting predominantly low-income countries and institutions. Here, a case is made for the use of free open source hardware in research and education, including countries and institutions where funds were never the biggest problem

Development and implementation of a significantly low-cost 3D bioprinter using recycled scrap material

The field of 3D bioengineering proposes to effectively contribute to the manufacture of artificial multicellular organ/tissues and the understanding of complex cellular mechanisms. In this regard, 3D cell cultures comprise a promising bioengineering possibility for the alternative treatment of organ function loss, potentially improving patient life expectancies. Patients with end-stage disease, for example, could benefit from treatment until organ transplantation or even undergo organ function restoration. Currently, 3D bioprinters can produce tissues such as trachea cartilage or artificial skin. Most low-cost 3D bioprinters are built from fused deposition modeling 3D printer frames modified for the deposition of biologically compatible material, ranging between $13.000,00 and$300.000,00. Furthermore, the cost of consumables should also be considered as they, can range from $3,85 and$100.000,00 per gram, making biomaterials expensive, hindering bioprinting access. In this context, our report describes the first prototype of a significantly low-cost 3D bioprinter built from recycled scrap metal and off-the-shelf electronics. We demonstrate the functionalized process and methodology proof of concept and aim to test it in different biological tissue scaffolds in the future, using affordable materials and open-source methodologies, thus democratizing the state of the art of this technology

Caracterização do desenvolvimento motor e equilíbrio corporal em indivíduos com deficiência intelectual e sua correlação com a idade cronológica / Caracterización del desarrollo motor y equilibrio corporal en personas con discapacidad intelectual y su correlación con la edad cronológica

A deficiência intelectual é definida pela Associação Americana de Deficiência Intelectual e Desenvolvimento (AAIDD) como limitações significativas no funcionamento intelectual, acompanhado de comprometimentos no comportamento adaptativo, expresso nas habilidades sociais, práticas e conceituais. Já desenvolvimento motor é um processo contínuo e sequencial que é iniciado na concepção e acompanha o indivíduo até a morte. Porém, diversos fatores, podem colocar em risco o curso normal do desenvolvimento de uma criança. Considerando que pessoas com deficiência intelectual, em geral, apresentam defasagens em várias áreas de seu desenvolvimento, elas demandam estímulos adequados para se desenvolverem. O objetivo deste estudo é avaliar a capacidade de equilíbrio por meio da Escala de Desenvolvimento Motor em indivíduos com deficiência intelectual de uma escola especializada no atendimento de alunos com deficiência, situada na região Metropolitana de Salvador correlacionando a idade cronológica com a idade motora desses alunos. O estudo apresenta um delineamento transversal com um grupo composto por 5 indivíduos diagnosticados com deficiência intelectual de ambos os sexos, sendo 4 meninos e 1 menina, com idades entre 7 e 11 anos. Durante o estudo todos os participantes foram avaliados apenas uma vez através da aplicação do teste de equilíbrio estático da Escala de Desenvolvimento Motor desenvolvida por Rosa Neto (2002). Verificou-se que a idade cronológica média da amostra foi de 112,6 meses e a idade motora para o equilíbrio foi de 52,8 meses, tendo classificação inferior e muito inferior. Os resultados do presente estudo apontam que indivíduos com deficiência intelectual demonstram atraso no desenvolvimento motor, principalmente no equilíbrio. Dessa forma, elas precisam de maior tempo para vivenciar determinadas atividades

Photography-based taxonomy is inadequate, unnecessary, and potentially harmful for biological sciences

The question whether taxonomic descriptions naming new animal species without type specimen(s) deposited in collections should be accepted for publication by scientific journals and allowed by the Code has already been discussed in Zootaxa (Dubois & Nemésio 2007; Donegan 2008, 2009; Nemésio 2009a–b; Dubois 2009; Gentile & Snell 2009; Minelli 2009; Cianferoni & Bartolozzi 2016; Amorim et al. 2016). This question was again raised in a letter supported by 35 signatories published in the journal Nature (Pape et al. 2016) on 15 September 2016. On 25 September 2016, the following rebuttal (strictly limited to 300 words as per the editorial rules of Nature) was submitted to Nature, which on 18 October 2016 refused to publish it. As we think this problem is a very important one for zoological taxonomy, this text is published here exactly as submitted to Nature, followed by the list of the 493 taxonomists and collection-based researchers who signed it in the short time span from 20 September to 6 October 2016

Impaired c-Fos and Polo-Like Kinase 2 Induction in the Limbic System of Fear-conditioned α-Synuclein Transgenic Mice

<div><p>α-Synuclein (αSYN) is genetically and neuropathologically linked to a spectrum of neurodegenerative diseases including Parkinson’s disease, dementia with Lewy bodies, and related disorders. Cognitive impairment is recapitulated in several αSYN transgenic mouse lines. However, the mechanisms of dysfunction in affected neurons are largely unknown. Here we measured neuronal activity induced gene products in the limbic system of αSYN transgenic mice upon fear conditioning (FC). Induction of the synaptic plasticity marker c-Fos was significantly reduced in the amygdala and hippocampus of (Thy1)-h[A30P]αSYN transgenic mice in an age-dependent manner. Similarly, the neuronal activity inducible polo-like kinase 2 (Plk2) that can phosphorylate αSYN at the pathological site serine-129 was up-regulated in both brain regions upon FC. Plk2 inductions were also significantly impaired in aged (Thy1)-h[A30P]αSYN transgenic mice, both in the amygdala and hippocampus. Plk2 inductions in the amygdala after FC were paralleled by a small but significant increase in the number of neuronal cell bodies immunopositive for serine-129 phosphorylated αSYN in young but not aged (Thy1)-h[A30P]αSYN transgenic mice. In addition, we observed in the aged hippocampus a distinct type of apparently unmodified transgenic αSYN profiles resembling synaptic accumulations of αSYN. Thus, the cognitive decline observed in aged αSYN transgenic mice might be due to impairment of neurotransmission and synaptic plasticity in the limbic system by distinct αSYN species.</p> </div

Transgenic human αSYN immunostaining in the hippocampus of (Thy1)-h[A30P]αSYN mice.

<p>Sections from old wt, young and old (Thy1)-h[A30P]αSYN transgenic mice were stained for human transgenic αSYN with the rat monoclonal antibody 15G7. As expected staining of tissue from old wt mice did not show any signal for human αSYN throughout the whole hippocampus (A–C). Tissue from young and old transgenic mice displayed a diffuse staining in the neuropil (D–I), and old transgenic mice showed some accumulation of human transgenic αSYN in the cytoplasm of neurons (G–I). Interestingly only the synaptic regions of the CA3 (I) and especially the CA1 (H) area of old transgenic mice were positive for transgenic αSYN positive dot-like structures (arrowhead in H). This staining pattern was not observed in similar areas of young transgenic mice (E,F). Size bars correspond to 20 µm.</p

c-Fos immunostaining in the amygdala of fear-conditioned (Thy1)-h[A30P]αSYN mice.

<p>Parallel mice as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0050245#pone-0050245-g001" target="_blank">Figure 1</a> were sacrificed within 40–60 min after FC training, brains dissected and amygdala sections stained with an antibody against c-Fos. Hardly any c-Fos immunoreactivity was observed in non-shocked mice under these conditions (A–I), whereas shock training induced c-Fos signals even in old non-transgenic mice (J–L). In contrast, young transgenic mice showed reduced c-Fos induction (M–O), which in the case of old (Thy1)-h[A30P]αSYN mice was so much impaired throughout the amygdala (P–R) that it failed to reach significance (S,T). ***p<0.0001; **p<0.001; *p<0.02. Size bars correspond to 20 µm. LA, lateral amygdala, BA, basal amygdala, CE, central nucleus.</p

Plk2 immunostaining in the hippocampus of fear-conditioned (Thy1)-h[A30P]αSYN mice.

<p>Mice were processed as described above and hippocampal sections stained with an antibody against Plk2. Compared to non-shocked mice (A–I), FC induced a Plk2 up-regulation in the hippocampal regions CA1, CA2, and CA3 of old non-transgenic mice (J–P) and young (Thy1)-h[A30P]αSYN mice (K–Q). This FC dependent up-regulation of Plk2 was significant for the old wt group (grey bars in S (**p<0.0066), T (**p<0.0024), U (*p<0.0169)) and the young transgenic mice (green bars in S (**p<0.0018), T (**p<0.0051), U (**p<0.0055)). Plk2 up-regulation was not seen in the hippocampal CA1, CA2 and CA3 regions of old transgenic mice (L–R) and failed to show any significance (yellow bars in S–U). Size bars correspond to 20 µm.</p

Impaired FC in aging (Thy1)-h[A30P]αSYN mice.

<p>The indicated groups of mice were trained and after 24 h assessed for context learning (A) and after another 6 h for cued learning (B). Compared to non-shocked control mice (light bars), age-matched old trained wild-type (wt) mice (gray bars) showed highly significant reductions of exploratory behavior in response to both context and cues. Young (Thy1)-h[A30P]αSYN transgenic (tg) mice (green bars) showed almost normal FC for context and showed significantly reduced exploratory behavior in cued FC when compared to old transgenic mice (yellow bars). The old transgenic mice showed much reduced context FC and no cued FC at all. ***p<0.0001; **p<0.01.</p